Aspirin, also known as acetylsalicylic acid, born on Mar. 6, 1899, is an antipyretic and analgesic medication with a long history. It is used to treat cold, fever, headache, toothache, arthralgia and rheumatism. Aspirin can also inhibit platelet aggregation, for preventing and treating ischemic heart disease, angina pectoris, cardiopulmonary infarction and cerebral thrombosis, it is also effective when used in blood vessel forming and bypass transplantation. It is the first anti-aggregation medication to be used for antithrombosis and has been established to treat acute myocardial infarction (AMI), unstable angina pectoris and for prevention of second-stage of myocardial infarction (MI). The principle of the anti-aggregation effect of aspirin is that aspirin inhibits the prostaglandin cyclooxygenase of platelets and prevents the synthesis of thromboxane A2 (TXA2) (TXA2 promotes aggregation of platelets). This effect is irreversible. Specifically, Aspirin irreversibly acetylates the hydroxyl of the 529 serine on the active peptide chain COX-1 of cyclooxygenase (COX) and inactivates COX. This inactivation blocks the conversion of arachidonic acid (AA) to thromboxane A2 (TXA2) and inhibits platelets (PLT) aggregation.
However, among patients who take Aspirin to prevent myocardial infarction and stroke, some people show a low aspirin response and a high incidence risk. The researchers consider that the main reason of the low response is that these patients have developed drug resistance against anticoagulation effect of aspirin. Among the cardiovascular disease patients taking Aspirin, patients with Aspirin resistance are three times more likely to develop myocardial infarction, stroke and even death compared to the others.
Therefore, the poor effect of using aspirin to inhibit platelet aggregation needs to be improved.